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Poster

Session: Session 1 Presenting Authors at Posters (Evens)

P-040 - How CSA1 integrates ETI cell death and PTI for full plant immunity

Tuesday, July 15, 2025
09:55 - 11:30  
Location: Confex Hall 3
Extracellular & Intracellular non-self recognition & signaling

 Two types of receptors mediate plant immunity – cell surface receptors and intracellular nucleotide-binding-leucin-rich repeat receptors (NLRs). This study investigates the role of the intracellular Arabidopsis NLR CONSTITUTIVE SHADE AVOIDANCE 1 (CSA1) in mediating cell death through its interactions with the receptor kinase BRASSINOSTEROID INSENSITIVE 1-ASSOCIATED RECEPTOR KINASE 1 (BAK1) INTERACTING RECEPTOR-LIKE KINASE 3 (BIR3). We demonstrated that CSA1 physically interacts with BIR3 but not directly with BAK1. It suppresses autoimmunity in bak1 bir3 double mutants suggesting a complex regulatory mechanism crucial for guarding BAK1 and BIR receptor complexes. Overexpression of the bacterial effector HopB1, known to cleave microbe-associated molecular pattern (MAMP)-activated BAK1, triggers cell death in a CSA1-dependent manner. MAMPs such as flg22 and pg23 enhance BAK1 cleavage, with pg23-induced cell death specifically reliant on CSA1. At the same time, typical pathogen-triggered immunity (PTI) responses are unaltered in the absence of CSA1. CSA1 is also required for cell death induced by BAK1 overexpression.  Here, we present novel results on how CSA1 is activated and contributes to pattern-triggered immunity by integrating cell surface receptor and intracellular NLR receptor-mediated defense responses for full plant immunity.